Current understanding of pathogenetic mechanisms in neuroendocrine neoplasms

Modica, Roberta; Liccardi, Alessia; Minotta, Roberto; Cannavale, Giuseppe; Benevento, Elio; Colao, Annamaria

doi:10.1080/17446651.2023.2279540

Cited by 7 publications

(2 citation statements)

References 160 publications

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“…The presence of chronic atrophic gastritis is pivotal in gastric NEN prognosis, whereas types 1 and 2 generally have a better prognosis than type 3 (which usually constitutes advanced disease at first presentation) [1,[18][19][20]. For example, Sheikh-Ahmad et al [21] conducted a single-centric study on patients with type 1 gastric NENs who were followed up for 41 months (between 11 and 288 months).…”

Section: Prognostic Markers and Multimodal Management Of Nensmentioning

confidence: 99%

Neuroendocrine Neoplasia: From Pathophysiology to Novel Therapeutic Approaches

Carsote,

Nistor

2024

Biomedicines

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Section: Prognostic Markers and Multimodal Management Of Nensmentioning

confidence: 99%

Neuroendocrine Neoplasia: From Pathophysiology to Novel Therapeutic Approaches

Carsote,

Nistor

2024

Biomedicines

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“…Secondarily, the co-presence of gastric, duodenal, and pancreatic neoplasia, in the majority of neuroendocrine tumors (NETs), represents a syndromic consequence via a common genetic background in multiple endocrine neoplasia (MEN) syndrome that comes with an increased burden of disease due to synchronous or asynchronous neoplasms requiring multidisciplinary management [ 11 , 12 , 13 ].…”

Section: Introductionmentioning

confidence: 99%

Turning Points in Cross-Disciplinary Perspective of Primary Hyperparathyroidism and Pancreas Involvements: Hypercalcemia-Induced Pancreatitis, MEN1 Gene-Related Tumors, and Insulin Resistance

Carsote,

Nistor,

Gheorghe

et al. 2024

IJMS

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We aimed to provide an in-depth analysis with respect to three turning points in pancreas involvement in primary hyperparathyroidism (PHP): hypercalcemia-induced pancreatitis (HCa-P), MEN1 (multiple endocrine neoplasia)-related neuroendocrine tumors (NETs), and insulin resistance (IR). This was a comprehensive review conducted via a PubMed search between January 2020 and January 2024. HCa-P (n = 9 studies, N = 1375) involved as a starting point parathyroid NETs (n = 7) or pancreatitis (n = 2, N = 167). Case report-focused analysis (N = 27) showed five cases of pregnancy PHP-HCa-P and three reports of parathyroid carcinoma (female/male ratio of 2/1, ages of 34 in women, men of 56). MEN1-NET studies (n = 7) included MEN1-related insulinomas (n = 2) or MEN1-associated PHP (n = 2) or analyses of genetic profile (n = 3), for a total of 877 MEN1 subjects. In MEN1 insulinomas (N = 77), the rate of associated PHP was 78%. Recurrence after parathyroidectomy (N = 585 with PHP) was higher after less-than-subtotal versus subtotal parathyroidectomy (68% versus 45%, p < 0.001); re-do surgery was 26% depending on surgery for pancreatic NETs (found in 82% of PHP patients). MEN1 pathogenic variants in exon 10 represented an independent risk factor for PHP recurrence. A single pediatric study in MEN1 (N = 80) revealed the following: a PHP rate of 80% and pancreatic NET rate of 35% and 35 underlying germline MEN1 pathogenic variants (and 3/35 of them were newly detected). The co-occurrence of genetic anomalies included the following: CDC73 gene variant, glucokinase regulatory protein gene pathogenic variant (c.151C>T, p.Arg51*), and CAH-X syndrome. IR/metabolic feature-focused analysis identified (n = 10, N = 1010) a heterogeneous spectrum: approximately one-third of adults might have had prediabetes, almost half displayed some level of IR as reflected by HOMA-IR > 2.6, and serum calcium was positively correlated with HOMA-IR. Vitamin D deficiency was associated with a higher rate of metabolic syndrome (n = 1). Normocalcemic and mildly symptomatic hyperparathyroidism (n = 6, N = 193) was associated with a higher fasting glucose and some improvement after parathyroidectomy. This multilayer pancreas/parathyroid analysis highlighted a complex panel of connections from pathogenic factors, including biochemical, molecular, genetic, and metabolic factors, to a clinical multidisciplinary panel.

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